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A Sting in the Tale of Th2 Immunity
Dario A. Gutierrez, Hans-Reimer Rodewald Immunity Volume 39, Issue 5, Pages (November 2013) DOI: /j.immuni Copyright © 2013 Elsevier Inc. Terms and Conditions
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Figure 1 Th2 Cell Immunity, IgE-Mediated Anaphylaxis, and IgE-Mediated Protection against Venoms IgE is the key effector immunoglobulin class that drives allergy and anaphylaxis (left arm). In this issue of Immunity, Marichal et al. (2013) and Palm et al. (2013) show that IgE can protect mice against venoms (middle arm). It is not clear how IgE mediates fundamentally opposing endpoints of protection versus allergy. This decision might be influenced by factors including dose of stimulus, species-specific immunoreactivity, tissue context (e.g., site of sting or contact with allergen), or the pathophysiological context, which might vastly differ between toxins and innocuous allergens. If the initial triggers of the Th2 cell response and the response itself are indistinguishable during allergy and protection, it is unclear how FcεRI-expressing effector cells, such as mast cells and basophils, can either provide protection against toxins or contribute to allergic diseases. Pathways leading to IgE production, which can be induced by allergens, toxins, and parasites or be promoted by perturbed tissue homeostasis (tissue stress), might all arise from the classical Th2-cell-mediated pathway (left and middle arms). However, alternative, less classical routes to IgE production have been reported and might contribute to IgE production in response to toxins and tissue damage (right arm). Immunity , DOI: ( /j.immuni ) Copyright © 2013 Elsevier Inc. Terms and Conditions
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